Journal articles: 'Defense signalling'

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Velusamy, Prema, Thangarajeswari Mohan, Divya Bhavani Ravi, S. N. Kishore Kumar, Ashokkumar Srinivasan, Lakshmi Narasimhan Chakrapani, Abhilasha Singh, Saradhadevi Varadharaj, and Periandavan Kalaiselvi. "Targeting the Nrf2/ARE Signalling Pathway to Mitigate Isoproterenol-Induced Cardiac Hypertrophy: Plausible Role of Hesperetin in Redox Homeostasis." Oxidative Medicine and Cellular Longevity 2020 (September 1, 2020): 1–13. http://dx.doi.org/10.1155/2020/9568278.

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Cardiac hypertrophy is the underlying cause of heart failure and is characterized by excessive oxidative stress leading to collagen deposition. Therefore, understanding the signalling mechanisms involved in excessive extracellular matrix deposition is necessary to prevent cardiac remodelling and heart failure. In this study, we hypothesized that hesperetin, a flavanone that elicits the activation of Nrf2 signalling and thereby suppresses oxidative stress, mediated pathological cardiac hypertrophy progression. A cardiac hypertrophy model was established with subcutaneous injection of isoproterenol in male Wistar rats. Oxidative stress markers, antioxidant defense status, and its upstream signalling molecules were evaluated to discover the impacts of hesperetin in ameliorating cardiac hypertrophy. Our results implicate that hesperetin pretreatment resulted in the mitigation of oxidative stress by upregulating antioxidant capacity of the heart. This curative effect might be owing to the activation of the master regulator of antioxidant defense system, known as Nrf2. Further, analysis of Nrf2 revealed that hesperetin enhances its nuclear translocation as well as the expression of its downstream targets (GCLC, NQO1, and HO-1) to boost the antioxidative status of the cells. To support this notion, in vitro studies were carried out in isoproterenol-treated H9c2 cells. Immunocytochemical analysis showed augmented nuclear localization of Nrf2 implicating the action of hesperetin at the molecular level to maintain the cellular redox homeostasis. Thus, it is conceivable that hesperetin could be a potential therapeutic candidate that enhances Nrf2 signalling and thereby ameliorates pathological cardiac remodelling.

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Krishnan, Anu, Limiya Joseph, and C. Bindu Roy. "An insight into Hevea - Phytophthora interaction: The story of Hevea defense and Phytophthora counter defense mediated through molecular signalling." Current Plant Biology 17 (January 2019): 33–41. http://dx.doi.org/10.1016/j.cpb.2018.11.009.

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Gómez, Margarita Ramírez, and Alia Rodríguez Villate. "Señales de reconocimiento entre plantas y hongos formadores de micorrizas arbusculares." Corpoica Ciencia y Tecnología Agropecuaria 11, no. 1 (June 30, 2010): 53. http://dx.doi.org/10.21930/rcta.vol11_num1_art:195.

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La asociación entre Hongo formadores de micorrizas arbusculares (HFMA) y las plantas ha permitido la adaptación de éstas a ecosistemas terrestres, presentándose en más del 80% de las plantas. El hospedero suministra carbohidratos al hongo y éste transporta los nutrientes que la planta requiere. El establecimiento de la simbiosis requiere procesos armónicos a nivel espacio-temporal, que dependen de señales específicas, para reconocimiento, colonización e intercambio de nutrientes. Las plantas presentan respuestas de defensa frente a la posible invasión de microorganismos, sin embargo, en la simbiosis éstas son débiles, localizadas y no impiden la colonización del hongo. Estas señales se observan en todas las etapas de la simbiosis, siendo la primera señal enviada por la planta en exudados de la raíz, especialmente en condiciones de bajo fósforo. Posteriormente los HFMA activan la expresión de genes que favorecen cambios a nivel celular para la formación del apresorio, del aparato de pre-penetración y en células de la corteza, del arbúsculo y la membrana periarbuscular, para el intercambio de nutrientes. Un aspecto de interés está relacionado con los mecanismos de atenuación de las respuestas de defensa de la planta. Se han planteado diversas hipótesis para entender este fenómeno y aunque el control de la simbiosis está regulado principalmente por la planta, aún se desconoce si los HFMA generan señales que facilitan el debilitamiento de las respuestas de defensa del hospedero. Este documento está orientado a hacer una revisión de las señales de reconocimiento HFMA - plantas para cada fase de la simbiosis, así como de algunos mecanismos de regulación de las respuestas de defensa de la planta para el establecimiento de la simbiosis. Recognition Signalling Between Arbuscular Mycorrhizal Fungi (AMF) and Plants The arbuscular mycorrhizal association has been instrumental for plant adaptation to terrestrial ecosystems over the last 400 million years. It is known that more than 80% of plant families form this symbiosis .Thus, nutrient exchange and protection from pathogens are thought to be key elements in the symbiosis. For the establishment of the association, harmonic processes for recognition, colonization and nutrients exchange are required both at temporal and space level. Plants react against microorganisms attack by producing defense responses, however, in the case of AM association, plant responses are weak, localized and do not stop colonization by the fungus. Signals are observed along the whole symbiosis process, being the first one produced by the plant through root exudates as a response for P stress. Then, AMF activate genes involved in plant cellular changes required for arbuscle formation, pre-penetration apparatus and at cortex level, the formation of periarbuscular membrane for the bi-directional nutrient exchange. Interestingly, several hypotheses have been formulated to explain the plant defense attenuation. For example, the activation of defense suppressors, the existence of plants with no defence responses to AMF and the existence of plants that suppress their defense response, among others. It is unknown whether the fungi induce low response levels from the host defense system. This document focuses on the signaling recognition between AMF and plants in each symbiosis phase and on the regulation mechanisms of the plant defense responses for the symbiosis establishment.

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Snedden, W., and S. Sakaluk. "The Effects of Acoustic Signalling on Male Spacing Behavior in the Sagebrush Cricket: Are Signals used in Territorial Defense?" UW National Parks Service Research Station Annual Reports 17 (January 1, 1993): 96–102. http://dx.doi.org/10.13001/uwnpsrc.1993.3159.

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Acoustic signalling in orthopterans functions in mate attraction and/or intermale spacing. The pattern of intermale distances should reflect the degree to which signalling functions in territorial defense. Males who are unable to detect, and thus respond to, the signals of rivals should be at greater risk of inadvertently intruding on the territories of rivals and of being intruded upon. We tested, in two field mark-recapture experiments with the sagebrush cricket Cyphoderris strepitans, the hypothesis that acoustic signals are used in intermale spacing, predicting that deafened males are compromised in their ability to repel rivals and should thus be found in closer proximity than control (hearing) males. There was no difference in mating success between deaf and control groups. There was a difference in nearest-neighbor distance between deaf and control animals in one replicate of one experiment and in one night of one replicate of the other experiment. These results suggest that calling has a sporadic effect on spacing behaviour of sagebrush crickets and thus primarily functions in mate attraction. The results are discussed in the context of the mating system of sagebrush crickets and the economics of territory defense.

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Mosblech, Alina, Sabine König, Irene Stenzel, Peter Grzeganek, Ivo Feussner, and Ingo Heilmann. "Phosphoinositide and Inositolpolyphosphate Signalling in Defense Responses of Arabidopsis thaliana Challenged by Mechanical Wounding." Molecular Plant 1, no. 2 (March 2008): 249–61. http://dx.doi.org/10.1093/mp/ssm028.

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Singh, Sunil Kumar, and Manisha Farsodia. "Polyamines Metabolism and their Relation with Reactive Oxygen Species and other Cellular Molecules during Plant Interactions with Pathogens." INTERNATIONAL JOURNAL OF PLANT AND ENVIRONMENT 4, no. 01 (January 31, 2018): 76–90. http://dx.doi.org/10.18811/ijpen.v4i01.12420.

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Polyamines are considered as essential molecules for plant growth and development. They are also implicated in abiotic and biotic stress responses. The roles of polyamines in abiotic stress regulation have been well understood, whereas their roles in response to biotic stress are poorly characterized in plants. However, various recent reports have acknowledged that polyamines and their catabolism generated H2O2 play important roles during biotic stress in plants. Polyamines and polyamines dependent signalling mediate reactive oxygen species (ROS) scavenging as these molecules accumulate in response to biotic stress. Polyamine catabolism also results in generation of H2O2 which act either by directly killing the pathogens or by acting as signalling molecules that mediate defense responses in plants. The H2O2 also interacts with the plant cell wall components and provides strength to the cell wall after infection and wounding. Polyamine catabolism generated H2O2 also play a role in signalling events post infection, which leads to hypersensitive cell death. They also interact with calcium dependent signalling cascade, phytohormones and secondary metabolites and provide resistance to plants during biotic stress. In this review we discussed the possible roles of polyamines and polyamines catabolism generated H2O2 and metabolites during plant host and pathogen interactions.

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Lu, Laifeng, Jianxu Wang, Ruiyu Zhu, Huangping Lu, Xiaodong Zheng, and Ting Yu. "Transcript profiling analysis of Rhodosporidium paludigenum-mediated signalling pathways and defense responses in mandarin orange." Food Chemistry 172 (April 2015): 603–12. http://dx.doi.org/10.1016/j.foodchem.2014.09.097.

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Bhattacharya, Ramcharan, Murali krishna Koramutla, Manisha Negi, Gregory Pearce, and Clarence A. Ryan. "Hydroxyproline-rich glycopeptide signals in potato elicit signalling associated with defense against insects and pathogens." Plant Science 207 (June 2013): 88–97. http://dx.doi.org/10.1016/j.plantsci.2013.03.002.

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Jeong, Mi-Ae, and Rae-Dong Jeong. "Resistance protein-mediated defense signalling in response to Turnip Crinkle Virus in Arabidopsis: recent advances." Journal of Plant Diseases and Protection 120, no. 3 (June 2013): 97–104. http://dx.doi.org/10.1007/bf03356460.

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Coppola, Lelio, Romanelli, Gualtieri, Molisso, Ruocco, Avitabile, et al. "Tomato Plants Treated with Systemin Peptide Show Enhanced Levels of Direct and Indirect Defense Associated with Increased Expression of Defense-Related Genes." Plants 8, no. 10 (October 3, 2019): 395. http://dx.doi.org/10.3390/plants8100395.

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Plant defense peptides represent an important class of compounds active against pathogens and insects. These molecules controlling immune barriers can potentially be used as novel tools for plant protection, which mimic natural defense mechanisms against invaders. The constitutive expression in tomato plants of the precursor of the defense peptide systemin was previously demonstrated to increase tolerance against moth larvae and aphids and to hamper the colonization by phytopathogenic fungi, through the expression of a wealth of defense-related genes. In this work we studied the impact of the exogenous supply of systemin to tomato plants on pests to evaluate the use of the peptide as a tool for crop protection in non-transgenic approaches. By combining gene expression studies and bioassays with different pests we demonstrate that the exogenous supply of systemin to tomato plants enhances both direct and indirect defense barriers. Experimental plants, exposed to this peptide by foliar spotting or root uptake through hydroponic culture, impaired larval growth and development of the noctuid moth Spodoptera littoralis, even across generations, reduced the leaf colonization by the fungal pathogen Botrytis cinerea and were more attractive towards natural herbivore antagonists. The induction of these defense responses was found to be associated with molecular and biochemical changes under control of the systemin signalling cascade. Our results indicate that the direct delivery of systemin, likely characterized by a null effect on non-target organisms, represents an interesting tool for the sustainable protection of tomato plants.

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Shumilina, Julia, Alena Kusnetsova, Alexander Tsarev, Henry C. Janse van Rensburg, Sergei Medvedev, Vadim Demidchik, Wim Van den Ende, and Andrej Frolov. "Glycation of Plant Proteins: Regulatory Roles and Interplay with Sugar Signalling?" International Journal of Molecular Sciences 20, no. 9 (May 13, 2019): 2366. http://dx.doi.org/10.3390/ijms20092366.

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Glycation can be defined as an array of non-enzymatic post-translational modifications of proteins formed by their interaction with reducing carbohydrates and carbonyl products of their degradation. Initial steps of this process rely on reducing sugars and result in the formation of early glycation products—Amadori and Heyns compounds via Schiff base intermediates, whereas their oxidative degradation or reactions of proteins with α-dicarbonyl compounds yield a heterogeneous group of advanced glycation end products (AGEs). These compounds accompany thermal processing of protein-containing foods and are known to impact on ageing, pathogenesis of diabetes mellitus and Alzheimer’s disease in mammals. Surprisingly, despite high tissue carbohydrate contents, glycation of plant proteins was addressed only recently and its physiological role in plants is still not understood. Therefore, here we summarize and critically discuss the first steps done in the field of plant protein glycation during the last decade. We consider the main features of plant glycated proteome and discuss them in the context of characteristic metabolic background. Further, we address the possible role of protein glycation in plants and consider its probable contribution to protein degradation, methylglyoxal and sugar signalling, as well as interplay with antioxidant defense.

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PEJSAK, ZYGMUNT, MARIAN TRUSZCZYŃSKI, and KAZIMIERZ TARASIUK. "Innate immunity against infectious diseases, particularly in swine." Medycyna Weterynaryjna 76, no. 2 (2020): 67–70. http://dx.doi.org/10.21521/mw.6369.

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The importance of innate defense mechanisms especially refering to swine, was characterized. Physical, chemical and microbial barriers were mentioned. The role of cells was underlined in controlling infection by phagocytosis without earlier immunisation by antigens and only depending on the genome of the born animal. The two main types of phagocytic cells were evaluated in antiinfectious activity: a)granular leucocytes, including neutrophils, basophils, eosynophils and mast cells, b)mononuclear phagocytes. These include blood circulating monocytes and macrophages. It was stated that natural killer cells belonging also to innate immune system can kill bacteria and viruses participating as etiologic agents in infectious diseases. Another group of innate immune factors, not cells but molecules, are creating defensins being host defense peptides. The complement mediates the inflammatory response, controlling bacterial infections. The following antiinfectious activity is exerted by Toll-like receptors. The presented cytokines are protein or glycoprotein molecules secreted by cells. They participate in intercellular and intracellular signalling.

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Ebel, Jürgen, Markus Feger, Ulrich Kissel, Axel Mithöfer, Tom Waldmüller, Arvind A. Bhagwat, and Eric G. Cosio. "Elicitor-binding proteins and signal transduction in the activation of a phytoalexin defense response." Canadian Journal of Botany 73, S1 (December 31, 1995): 506–10. http://dx.doi.org/10.1139/b95-289.

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Inducible plant defenses against potential pathogens are thought to be activated by signal compounds released during early stages of the infection process. In the incompatible interaction between soybean (Glycine max L.) and the oomycete Phytophthora megasperma f.sp. glycinea (= Phytophthora sojae) a rapid, localized phytoalexin response is activated at the level of transcription. The phytoalexin response is also stimulated in various soybean tissues, including cultured cells, following treatment with an elicitor derived from the cell walls of the fungus. The best characterized elicitors of P. megasperma for soybean are the branched (1→3)- and (1→6)-linked β-glucans, structural polysaccharides of the hyphal walls. The glucans are naturally released during the early stages of germination of the fungal cysts in a host-independent manner. Cyclic β-glucans of Bradyrhizobium japonicum USDA 110, a symbiont of soybean, arc not active in inducing phytoalexin production in soybean. When tested in combination, B. japonicum β-glucans inhibited stimulation of phytoalexin accumulation by the fungal glucans. Surface-localized glucan-binding proteins exist in soybean cells that display high affinity and specificity for the fungal β-glucans, including an elicitor-active hepta-β-glucoside fragment derived from the polysaccharide, suggesting that elicitor action involves a transmembrane signalling process. The main component of the soybean β-glucan binding sites appears to be a 70-kDa protein. Hepta-β-glucoside binding sites exist in several other legumes, such as bean (Phaseolus vulgaris L.), pea (Pisum sativum L.), and lupine (Lupinus albus L.). The signalling process initiated by the β-glucan elicitor, which leads to the activation of the phytoalexin defense response in soybean, involves changes in the permeability of the plasma membrane to Ca2+ and H+. Chloride channel antagonists are more efficient than calcium channel antagonists in inhibiting both the phytoalexin response and the inducible ion fluxes. The results present evidence that the observed permeability changes of the plasma membrane are primary events in the transduction of the elicitor signal(s) by the challenged soybean cells. Key words: soybean (Glycine max), Phytophthora megasperma f.sp. glycinea, β-glucan elicitor, elicitor-binding proteins, phytoalexins, Ca2+.

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Pedras, M. Soledade C., and Q. Huy To. "Defense and signalling metabolites of the crucifer Erucastrum canariense : Synchronized abiotic induction of phytoalexins and galacto-oxylipins." Phytochemistry 139 (July 2017): 18–24. http://dx.doi.org/10.1016/j.phytochem.2017.03.005.

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Gao, Jin, Yaoxin Zhang, Zhengguo Li, and Mingchun Liu. "Role of ethylene response factors (ERFs) in fruit ripening." Food Quality and Safety 4, no. 1 (January 3, 2020): 15–20. http://dx.doi.org/10.1093/fqsafe/fyz042.

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Abstract The ethylene response factors (ERFs) belong to the APETALA2/ethylene response factor (AP2/ERF) superfamily and act downstream of the ethylene signalling pathway to regulate the expression of ethylene responsive genes. In different species, ERFs have been reported to be involved in plant development, flower abscission, fruit ripening, and defense responses. In this review, based on the new progress made by recent studies, we summarize the specific role and mode of action of ERFs in regulating different aspects of ripening in both climacteric and non-climacteric fruits, and provide new insights into the role of ethylene in non-climacteric fruit ripening.

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Varin, Audrey, Subhankar Mukhopadhyay, Georges Herbein, and Siamon Gordon. "Alternative activation of macrophages by IL-4 impairs phagocytosis of pathogens but potentiates microbial-induced signalling and cytokine secretion." Blood 115, no. 2 (January 14, 2010): 353–62. http://dx.doi.org/10.1182/blood-2009-08-236711.

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Abstract Alternatively activated macrophages play an important role in host defense in the context of a T helper type 2 (Th2) microenvironment such as parasitic infection. However, the role of these macrophages during secondary challenge with Th1 pathogens is poorly defined. In this study, thioglycollate-elicited mouse peritoneal macrophages were treated with interleukin-4 (IL-4) or IL-13 in vitro and challenged with Neisseria meningitidis. After 8 to 12 hours of IL-4 pretreatment, the nonopsonic phagocytic uptake of N meningitidis was markedly reduced, depending on the common IL-4Rα chain, but independent of Scavenger receptor A and macrophage receptor with collagenous structure (MARCO), 2 known receptors for N meningitidis. Inhibition of phagocytosis extended to several other microbial particles, zymosan, and other bacteria. Concomitantly, IL-4 potentiated the secretion of proinflammatory cytokines, after additional bacterial stimulation, which depended on the MyD88 signaling pathway. Similar results were obtained after intraperitoneal stimulation of IL-4 and N meningitidis in vivo. Further in vitro studies showed a striking correlation with inhibition of Akt phosphorylation and stimulation of the mitogen-activated protein kinase pathway; inhibition of phagocytosis was associated with inhibition of phagosome formation. These findings are relevant to host defense in mixed infections within a Th2 microenvironment and shed light on immunologic functions associated with alternative priming and full activation of macrophages.

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Didcock, L., D. F. Young, S. Goodbourn, and R. E. Randall. "The V Protein of Simian Virus 5 Inhibits Interferon Signalling by Targeting STAT1 for Proteasome-Mediated Degradation." Journal of Virology 73, no. 12 (December 1, 1999): 9928–33. http://dx.doi.org/10.1128/jvi.73.12.9928-9933.1999.

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ABSTRACT To replicate in vivo, viruses must circumvent cellular antiviral defense mechanisms, including those induced by the interferons (IFNs). Here we demonstrate that simian virus 5 (SV5) blocks IFN signalling in human cells by inhibiting the formation of the IFN-stimulated gene factor 3 and gamma-activated factor transcription complexes that are involved in activating IFN-α/β- and IFN-γ-responsive genes, respectively. SV5 inhibits the formation of these complexes by specifically targeting STAT1, a component common to both transcription complexes, for proteasome-mediated degradation. Expression of the SV5 structural protein V, in the absence of other virus proteins, also inhibited IFN signalling and induced the degradation of STAT1. Following infection with SV5, STAT1 was degraded in the absence of virus protein synthesis and remained undetectable for up to 4 days postinfection. Furthermore, STAT1 was also degraded in IFN-pretreated cells, even though the cells were in an antiviral state. Since pretreatment of cells with IFN delayed but did not prevent virus replication and protein synthesis, these observations suggest that following infection of IFN-pretreated cells, SV5 remains viable within the cells until they eventually go out of the antiviral state.

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Lievens, Dirk, Wouter Eijgelaar, Erik Biessen, Mat Daemen, and Esther Lutgens. "The multi-functionality of CD40L and its receptor CD40 in atherosclerosis." Thrombosis and Haemostasis 102, no. 08 (2009): 206–14. http://dx.doi.org/10.1160/th09-01-0029.

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SummaryDisrupting the CD40-CD40L co-stimulatory pathway reduces atherosclerosis and induces a stable atherosclerotic plaque phenotype that is low in inflammation and high in fibrosis. Therefore, inhibition of the CD40-CD40L pathway is an attractive therapeutic target to reduce clinical complications of atherosclerosis. The CD40-CD40L dyad is known to interact with other costimulatory molecules, to activate antigen-presenting cells (APC) and to contribute to T-cell priming and B-cell isotype switching. Besides their presence on T-cells and APCs, CD40 and CD40L are also present on macrophages, endothelial cells and vascular smooth muscle cells in the plaque, where they can exert pro-atherogenic functions. Moreover, recent progress indicates the involvement of neutrophil CD40, platelet CD40L and dendritic cell CD40 in atherogenesis. Since systemic CD40-CD40L modulation compromises host defense, more targeted interventions are needed to develop superior treatment strategies for atherosclerosis. We believe that by unravelling the cell-cell CD40-CD40L interactions, inhibition of cell-type specific (signalling components of) CD40(L) that do not compromise the patient’s immune system, will become possible. In this review, we highlight the cell-type specific multi-functionality of CD40-CD40L signalling in atherosclerosis.

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Wyżewski, Zbigniew, Marcin Gradowski, Marianna Krysińska, Małgorzata Dudkiewicz, and Krzysztof Pawłowski. "A novel predicted ADP-ribosyltransferase-like family conserved in eukaryotic evolution." PeerJ 9 (March 10, 2021): e11051. http://dx.doi.org/10.7717/peerj.11051.

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The presence of many completely uncharacterized proteins, even in well-studied organisms such as humans, seriously hampers full understanding of the functioning of the living cells. ADP-ribosylation is a common post-translational modification of proteins; also nucleic acids and small molecules can be modified by the covalent attachment of ADP-ribose. This modification, important in cellular signalling and infection processes, is usually executed by enzymes from the large superfamily of ADP-ribosyltransferases (ARTs). Here, using bioinformatics approaches, we identify a novel putative ADP-ribosyltransferase family, conserved in eukaryotic evolution, with a divergent active site. The hallmark of these proteins is the ART domain nestled between flanking leucine-rich repeat (LRR) domains. LRRs are typically involved in innate immune surveillance. The novel family appears as putative novel ADP-ribosylation-related actors, most likely pseudoenzymes. Sequence divergence and lack of clearly detectable “classical” ART active site suggests the novel domains are pseudoARTs, yet atypical ART activity, or alternative enzymatic activity cannot be excluded. We propose that this family, including its human member LRRC9, may be involved in an ancient defense mechanism, with analogies to the innate immune system, and coupling pathogen detection to ADP-ribosyltransfer or other signalling mechanisms.

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Brandt, Claus, and Bente K. Pedersen. "The Role of Exercise-Induced Myokines in Muscle Homeostasis and the Defense against Chronic Diseases." Journal of Biomedicine and Biotechnology 2010 (2010): 1–6. http://dx.doi.org/10.1155/2010/520258.

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Chronic inflammation is involved in the pathogenesis of insulin resistance, atherosclerosis, neurodegeneration, and tumour growth. Regular exercise offers protection against type 2 diabetes, cardiovascular diseases, colon cancer, breast cancer, and dementia. Evidence suggests that the protective effect of exercise may to some extent be ascribed to the antiinflammatory effect of regular exercise. Here we suggest that exercise may exert its anti-inflammatory effect via a reduction in visceral fat mass and/or by induction of an anti-inflammatory environment with each bout of exercise. According to our theory, such effects may in part be mediated via muscle-derived peptides, so-called “myokines”. Contracting skeletal muscles release myokines with endocrine effects, mediating direct anti-inflammatory effects, and/or specific effects on visceral fat. Other myokines work locally within the muscle and exert their effects on signalling pathways involved in fat oxidation and glucose uptake. By mediating anti-inflammatory effects in the muscle itself, myokines may also counteract TNF-driven insulin resistance. In conclusion, exercise-induced myokines appear to be involved in mediating both systemic as well as local anti-inflammatory effects.

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Marquis, Valentin, Ekaterina Smirnova, Laure Poirier, Julie Zumsteg, Fabian Schweizer, Philippe Reymond, and Thierry Heitz. "Stress‐ and pathway‐specific impacts of impaired jasmonoyl‐isoleucine (JA‐Ile) catabolism on defense signalling and biotic stress resistance." Plant, Cell & Environment 43, no. 6 (March 25, 2020): 1558–70. http://dx.doi.org/10.1111/pce.13753.

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E. King, Michael, Samuel Miller, Reuben F. Burch V, Will Reimann, Jon Shalala, Anthony Piroli, Cory Bichey, and Ted Rath. "Quantification of Information Transmission in Signal Play-calling for NCAA Division 1 College Football: A Comprehensive Literature Review." International Journal of Kinesiology and Sports Science 9, no. 1 (January 31, 2021): 24. http://dx.doi.org/10.7575/aiac.ijkss.v.9n.1p.24.

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Background: To gain a competitive advantage in National Collegiate Athletic Association (NCAA) Division 1 American college football, teams often use a coded, hand/body gesture-based play-calling system to communicate calls to student-athletes on the field. Objective: The purpose of this study is to apply cognitive engineering concepts toward the improvement of signal transmission such that a realistic amount of data signaled will be received and understood by the student-athlete. Methods: Partnering with an NCAA coaching staff, information transmitted via signal-based communication pathways were quantified to inform the design of their signal system. Quality control coaches, practitioners of football signalling characterization and design, used an autoethnographic frame to train researchers on the communication protocol standards. A comprehensive literature review of sources from 1900 to 2019 was conducted to examine information transmission, signal-gesture taxonomies, sign-language recognition, and code design. Findings were applied to the signal system to quantify the information contained in the transmission between the signalling coaches and the student-athletes. Results: Results found that the observed signal system transmits an average of 12.62 bits of information on offense and 12.92 bits on defense with 23% and 12% redundancy, respectively. Conclusion: Recommendations were provided to the coaching staff regarding code optimization and gesture design to improve student-athlete performance.

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Stack, Julianne, Ismar R. Haga, Martina Schröder, Nathan W. Bartlett, Geraldine Maloney, Patrick C. Reading, Katherine A. Fitzgerald, Geoffrey L. Smith, and Andrew G. Bowie. "Vaccinia virus protein A46R targets multiple Toll-like–interleukin-1 receptor adaptors and contributes to virulence." Journal of Experimental Medicine 201, no. 6 (March 14, 2005): 1007–18. http://dx.doi.org/10.1084/jem.20041442.

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Viral immune evasion strategies target key aspects of the host antiviral response. Recently, it has been recognized that Toll-like receptors (TLRs) have a role in innate defense against viruses. Here, we define the function of the vaccinia virus (VV) protein A46R and show it inhibits intracellular signalling by a range of TLRs. TLR signalling is triggered by homotypic interactions between the Toll-like–interleukin-1 resistance (TIR) domains of the receptors and adaptor molecules. A46R contains a TIR domain and is the only viral TIR domain–containing protein identified to date. We demonstrate that A46R targets the host TIR adaptors myeloid differentiation factor 88 (MyD88), MyD88 adaptor-like, TIR domain–containing adaptor inducing IFN-β (TRIF), and the TRIF-related adaptor molecule and thereby interferes with downstream activation of mitogen-activated protein kinases and nuclear factor κB. TRIF mediates activation of interferon (IFN) regulatory factor 3 (IRF3) and induction of IFN-β by TLR3 and TLR4 and suppresses VV replication in macrophages. Here, A46R disrupted TRIF-induced IRF3 activation and induction of the TRIF-dependent gene regulated on activation, normal T cell expressed and secreted. Furthermore, we show that A46R is functionally distinct from another described VV TLR inhibitor, A52R. Importantly, VV lacking the A46R gene was attenuated in a murine intranasal model, demonstrating the importance of A46R for VV virulence.

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Shanahan, Fergus. "Physiological Basis for Novel Drug Therapies Used to Treat the Inflammatory Bowel Diseases I. Pathophysiological basis and prospects for probiotic therapy in inflammatory bowel disease." American Journal of Physiology-Gastrointestinal and Liver Physiology 288, no. 3 (March 2005): G417—G421. http://dx.doi.org/10.1152/ajpgi.00421.2004.

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Mechanisms underlying the conditioning influence of the intestinal flora on mucosal homeostasis, including development and function of immune responses, are attracting increasing scientific scrutiny. The intestinal flora is a positive asset to host defense, but some of its components may, in genetically susceptible hosts, become a risk factor for development of inflammatory bowel disease (IBD). It follows that strategies to enhance assets or offset microbial liabilities represent a therapeutic option; therein lies the rationale for manipulation of the flora in IBD. In addition, the diversity of regulatory signalling among the flora and host epithelum, lymphoid tissue, and neuromuscular apparatus is an untapped reservoir from which novel therapeutics may be mined. Moreover, the capacity to engineer food-grade or commensal bacteria to deliver therapeutic molecules to the intestinal mucosa promises to extend the scope of microbial manipulation for the benefit of mankind.

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Eichhorn, Tanja, Michael B. Fischer, and Viktoria Weber. "Mechanisms of Endothelial Activation in Sepsis and Cell Culture Models to Study the Heterogeneous Host Response." International Journal of Artificial Organs 40, no. 1 (January 2017): 9–14. http://dx.doi.org/10.5301/ijao.5000560.

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Sepsis is currently viewed as a fundamental disintegration of control functions from intracellular signalling to immunoregulatory and neuroendocrine mechanisms. The immediate threat in sepsis is invasive infection, and the need to activate immune defense mechanisms to clear the pathogen before irreparable damage occurs. In the process of pathogen elimination, however, the systemic host response to infection may cause collateral damage to the endothelium and may lead to the destruction of host tissues. A number of experimental models have been developed to monitor endothelial activation and to study endothelial dysfunction under septic conditions. Here, we review the application of these models to assess the highly variable host response in sepsis and to investigate the efficacy of adsorbent-based extracorporeal therapies. We also highlight the need for efficient diagnostic tools, which are indispensable to select patients who are likely to benefit from distinct adjunctive therapies.

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Thuerig, Barbara, Georg Felix, Andres Binder, Thomas Boller, and Lucius Tamm. "An extract of Penicillium chrysogenum elicits early defense-related responses and induces resistance in Arabidopsis thaliana independently of known signalling pathways." Physiological and Molecular Plant Pathology 67, no. 3-5 (September 2005): 180–93. http://dx.doi.org/10.1016/j.pmpp.2006.01.002.

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Mathur, Piyush, Ved Pal Singh, and Rupam Kapoor. "Interactive effects of CO2 concentrations and Alternaria brassicae (Berk.) Sacc. infection on defense signalling in Brassica juncea (L.) Czern. & Coss." European Journal of Plant Pathology 151, no. 2 (November 16, 2017): 413–25. http://dx.doi.org/10.1007/s10658-017-1382-7.

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Hrunyk, Nataliya, Roman Gout, and Valentina Kovaleva. "Regulation of gene expression for defensins and lipid transfer protein in Scots pine seedlings by necrotrophic pathogen Alternaria alternata (Fr.)." Folia Forestalia Polonica 59, no. 2 (June 27, 2017): 152–58. http://dx.doi.org/10.1515/ffp-2017-0015.

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AbstractDamping-off disease in pine seedling, caused by fungi and oomycetes (Fusarium, Alternaria, Botrytis, Phytophthora) and other species, is one of the most dangerous diseases in conifer nurseries and greenhouses worldwide. Alternaria alternata is a necrotrophic pathogen, which causes early blight in higher plants and results in massive economic losses in agro-industry as well as in forestry. Pine seedlings that lack strong lignificated and suberized cell walls at early stages of their growth are vulnerable to damping-off disease. So, triggering the synthesis of antimicrobial compounds, such as phytoalexins, anticipins and pathogenesis-related (PR) proteins, is the main defense strategy to confine pathogens at early stages of pine ontogenesis. Defensins and lipid transfer proteins are members of two PR-protein families (PR-12 and PR-14 respectively) and possess antimicrobial activities in vitro through contact toxicity, and the involvement in defense signalling. In this work, we describe the changes in the expression levels of four defensin genes and lipid transfer protein in Scots pine seedlings infected with A. alternata. The expression levels of PsDef1 and PsDef2 increased at 48 h.p.i. (hours post inoculation). The levels of PsDef4 transcripts have increased after 6 and 24 hours. Notably, at 48 h.p.i., the level of PsDef4 transcripts was decreased by 1.2 times compared to control. The level of PsDef3 transcripts was reduced at all three time points. On the other hand, the level of PsLTP1 transcripts increased at 6 h and 48 h.p.i.; while at 24 h.p.i., it decreased by 20% when compared to the control sample. Our results suggest that defensins and lipid transfer protein are involved in the defense response of young Scots pine to necrotrophic pathogen. Thus, those genes can be used as the molecular markers in forestry selection and development of the ecologically friendly remedies for coniferous seedlings cultivation in greenhouses and nurseries.

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Lua, B. L., and B. C. Low. "Filling the GAPs in cell dynamics control: BPGAP1 promotes cortactin translocation to the cell periphery for enhanced cell migration." Biochemical Society Transactions 32, no. 6 (October 26, 2004): 1110–12. http://dx.doi.org/10.1042/bst0321110.

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Cells undergo dynamic changes in morphology or motility during cellular division and proliferation, differentiation, neuronal pathfinding, wound healing, apoptosis, host defense and organ development. These processes are controlled by signalling events relayed through cascades of protein interactions leading to the establishment and maintenance of cytoskeletal networks of microtubules and actin. Various regulators, including the Rho small GTPases (guanine nucleotide triphosphatases), serve as master switches to fine-tune the amplitude, duration as well as the integration of such circuitry responses. Rho GTPases are activated by guanine nucleotide-exchange factors and inactivated by GAPs (GTPase-activating proteins). Although normally down-regulating signalling pathways by catalysing their GTPase activity, many GAPs exist with various protein modules, the functions of which still largely remain unknown. BPGAP1 is a novel RhoGAP that co-ordinately regulates pseudopodia and cell migration through the interplay of its BNIP-2 and Cdc42GAP homology domains serving as a homophilic/heterophilic interaction device, an enzymic RhoGAP domain that inactivates RhoA and a proline-rich region that binds the Src homology-3 domain of cortactin. Both proteins co-localize to cell periphery and enhance cell migration. As a molecular scaffold in cortical actin assembly and organization, cortactin and its interaction with small GTPases, GAPs and tyrosine kinases seems set to provide further insights to the multiplicity and complexity of cell dynamics control. Elucidating how these processes might be individually or co-ordinately regulated through cortactin remains an exciting future challenge.

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JOHNSON, N., A. HITCHMAN, D. PHAN, and L. SMITH. "Self-exciting point process models for political conflict forecasting." European Journal of Applied Mathematics 29, no. 4 (December 4, 2017): 685–707. http://dx.doi.org/10.1017/s095679251700033x.

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In 2008, the Defense Advanced Research Project Agency commissioned a database known as the Integrated Crisis Early Warning System to serve as the foundation for models capable of detecting and predicting increases in political conflict worldwide. Such models, by signalling expected increases in political conflict, would help inform and prepare policymakers to react accordingly to conflict proliferation both domestically and internationally. Using data from the Integrated Crisis Early Warning System, we construct and test a self-exciting point process, or Hawkes process, model to describe and predict amounts of domestic, political conflict; we focus on Colombia and Venezuela as examples for this model. By comparing the accuracy of fitted models to the observed data, we find that we are able to closely describe occurrences of conflict in each country. Thus, using this model can allow policymakers to anticipate relative increases in the amount of domestic political conflict following major events.

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Yan, T., F. Zhang, Y. He, X. Wang, X. Jin, P. Zhang, and D. Bi. "Enterococcus faeciumHDRsEf1 elevates the intestinal barrier defense against enterotoxigenicEscherichia coliand regulates occludin expression via activation of TLR-2 and PI3K signalling pathways." Letters in Applied Microbiology 67, no. 5 (September 24, 2018): 520–27. http://dx.doi.org/10.1111/lam.13067.

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Schmidt, Axel, Raimund Nagel, Trygve Krekling, Erik Christiansen, Jonathan Gershenzon, and Paal Krokene. "Induction of isoprenyl diphosphate synthases, plant hormones and defense signalling genes correlates with traumatic resin duct formation in Norway spruce (Picea abies)." Plant Molecular Biology 77, no. 6 (October 15, 2011): 577–90. http://dx.doi.org/10.1007/s11103-011-9832-7.

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Gęgotek, Agnieszka, Pedro Domingues, and Elżbieta Skrzydlewska. "Natural Exogenous Antioxidant Defense against Changes in Human Skin Fibroblast Proteome Disturbed by UVA Radiation." Oxidative Medicine and Cellular Longevity 2020 (November 5, 2020): 1–12. http://dx.doi.org/10.1155/2020/3216415.

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Daily exposure of the skin to UVA radiation causes oxidative modifications to cellular components and biomolecules. These include proteins involved in the metabolism and cytoprotection of fibroblasts, and their modification can contribute to the disruption of cell function and the development of skin disorders. Therefore, there remains a need for highly active cytoprotective compounds with antioxidant properties. The purpose of this study was to investigate the effect of ascorbic acid on the activity of rutin against UVA-induced changes in the proteome of human fibroblasts. All analyses were carried out on fibroblasts cultured in a three-dimensional system exposed to UVA radiation and incubated with rutin and ascorbic acid. Their proteomic profile was analyzed using nano-HPLC, which revealed 150 proteins whose expression was significantly altered between treatment conditions. UVA radiation led to changes in the expression of 82 proteins. However, some of these changes were mitigated by rutin and ascorbic acid separately (23 and 25 proteins, respectively) and rutin and ascorbic acid together (23 proteins). UVA radiation has led to the upregulation of proteins involved in gene expression, catalytic processes and antioxidant pathways, and downregulation of proteins with binding activity. Nevertheless, rutin and ascorbic acid used separately or together have countered these changes to varying degrees. Moreover, rutin and ascorbic acid stimulated fibroblasts irradiated by UVA to increase the expression of the signalling molecules responsible for the opening of the transmembrane channels. In the context of the results obtained, the observed cytoprotective effect of the cooperation of rutin and ascorbic acid results not only from the overlapping properties of the compounds. The effect of rutin alone is probably inhibited by its limited bioavailability. Therefore, its interaction with ascorbic acid increases membrane penetration and improves the cytoprotective effect on skin fibroblasts.

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Weksberg, David C., Carl G. Feng, Alan Sher, and Margaret A. Goodell. "The P47 GTPase Lrg-47 Links Host Defense and HSC Proliferation." Blood 110, no. 11 (November 16, 2007): 640. http://dx.doi.org/10.1182/blood.v110.11.640.640.

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Abstract Hematopoietic stem cells (HSCs) are largely quiescent, self-renewing cells that give rise to all adult blood lineages. They have a remarkable capacity to respond to proliferative stimuli from a variety of insults, exiting their quiescent phase and undergoing a period of self-renewal and differentiation in order to restore hematopoietic homeostasis. Yet, while some molecular controls on the cycle of HSC activation and quiescence have been elucidated, little is known about the mechanisms linking this process to natural signals, such as the stress of an immune response to chronic infection. Previous work in our laboratory examined gene expression changes in a cycle of activation, expansion, and return to quiescence in HSCs stimulated by the chemotherapeutic agent 5-fluorouracil (5FU). One family of genes identified by this approach encodes the interferon-inducible p47 GTPases, which has been previously characterized solely in the context of the immune response to intracellular infections. Interestingly, mice deficient for one member of this family, Lrg-47, had been observed to develop a major hematopoietic defect in the face of infectious challenge. This combination of findings led us to test the novel hypothesis that Lrg-47 might regulate HSC function in the face of either chemical or pathogenic stress. We found that, while Lrg-47 −/ − mice have largely normal blood counts under homeostasis, these animals exhibited impaired hematopoietic recovery from stress in the form of sublethal irradiation or 5FU treatment. Furthermore, we show that HSCs deficient in Lrg-47 are profoundly compromised in functional repopulation assays, even when given extreme advantages over competitor marrow. We also observed, in BrdU labeling studies, that Lrg-47 −/ − HSCs display dysregulated HSC proliferation, with substantially increased turnover at baseline. We found that this inappropriate proliferation has a functional consequence, as Lrg-47 −/ − mice have a delayed expansion of the HSC compartment following 5FU treatment. Finally, in order to investigate the response of stem and progenitor populations to infectious stimuli, we challenged mice by infection with Mycobacterium avium. Phenotypic and functional assays demonstrated that, while wild-type progenitors expand dramatically in response to infection, Lrg-47 −/ − mice show a stark defect. Our findings thus point to a dual role for Lrg-47 - first as an inhibitor of HSC proliferation in the steady state, and second as a key regulator of HSCs in the response to injury. Overall, our results establish a link between the response to infection and HSC activation, and demonstrate a novel function for a member of the p47GTPase family. Additionally, as Lrg-47 has been chiefly known as an effector of IFNgamma signalling, our results suggest a possible mechanism for the inhibitory effects of this cytokine on hematopoiesis, with implications for human diseases with interferon-related pathogenesis. Most generally, our findings reveal an unexpected intersection point between the fields of stem cell biology and the immune response to pathogens, and suggest that defects in HSC function should be considered as possible determinants of host susceptibility to infection.

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Rosenthal, Kenneth L. "Tweaking Innate Immunity: The Promise of Innate Immunologicals as Anti-Infectives." Canadian Journal of Infectious Diseases and Medical Microbiology 17, no. 5 (2006): 307–14. http://dx.doi.org/10.1155/2006/195957.

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New and exciting insights into the importance of the innate immune system are revolutionizing our understanding of immune defense against infections, pathogenesis, and the treatment and prevention of infectious diseases. The innate immune system uses multiple families of germline-encoded pattern recognition receptors (PRRs) to detect infection and trigger a variety of antimicrobial defense mechanisms. PRRs are evolutionarily highly conserved and serve to detect infection by recognizing pathogen-associated molecular patterns that are unique to microorganisms and essential for their survival. Toll-like receptors (TLRs) are transmembrane signalling receptors that activate gene expression programs that result in the production of proinflammatory cytokines and chemokines, type I interferons and antimicrobial factors. Furthermore, TLR activation facilitates and guides activation of adaptive immune responses through the activation of dendritic cells. TLRs are localized on the cell surface and in endosomal/lysosomal compartments, where they detect bacterial and viral infections. In contrast, nucleotide-binding oligomerization domain proteins and RNA helicases are located in the cell cytoplasm, where they serve as intracellular PRRs to detect cytoplasmic infections, particularly viruses. Due to their ability to enhance innate immune responses, novel strategies to use ligands, synthetic agonists or antagonists of PRRs (also known as 'innate immunologicals') can be used as stand-alone agents to provide immediate protection or treatment against bacterial, viral or parasitic infections. Furthermore, the newly appreciated importance of innate immunity in initiating and shaping adaptive immune responses is contributing to our understanding of vaccine adjuvants and promises to lead to improved next-generation vaccines.

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Kuzmenko, D. I., P. G. Burov, V. Yu Serebrov, E. A. Fait, and T. V. Perevozchikova. "Functional state of a sphingomyeline cycle and free radical lipid oxidation activity of a rat's liver during different phases of starvation." Biomeditsinskaya Khimiya 58, no. 5 (2012): 556–63. http://dx.doi.org/10.18097/pbmc20125805556.

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The functional state of a sphingomyeline cycle and character of its mutual relations with the processes of free radical lipid oxidation during starvation of animals without any restriction of access to drinking water at 1, 2, 3 day (I phase) and 6 day (II phase of starvation) were studied at the liver of rats. The maximal values of the ceramide/sphingomyeline ratio and activity neutral sphingomyelinase and executive caspase-3 were reached in a liver of animals at the 3rd day of starvation . From the 3rd day of starvation the concentration of the tumour necrosis factor-α which is one of activators neutral sphingomyelinase was increase in rats blood serum. During the extent of large part of the I phase of starvation the intensity of free radical lipid peroxidation in a liver had almost the same level as in control group - that was a result of the high-grade functioning of antioxidant defense system. After transition the I phase of starvation into the II phase (6 day of experiment) the oxidative stress was developed as result of an exhaustion of system antioxidant defense potential in a liver. The results of this data can testify that during I phase of starvation in a liver the conditions was raised for display of the ceramide-mediated proapoptotic signalling. We assume that ceramide-mediated apoptosis is one of mechanisms of optimization of liver cellular population at the frames of metabolic adaptation. The I phase of starvation in a liver proves by the ceramide-mediated proapoptotic signaling developing. During the II phase of starvation the oxidative stress process were prevailed.

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Stenvinkel, Peter, Colin J. Meyer, Geoffrey A. Block, Glenn M. Chertow, and Paul G. Shiels. "Understanding the role of the cytoprotective transcription factor nuclear factor erythroid 2-related factor 2—lessons from evolution, the animal kingdom and rare progeroid syndromes." Nephrology Dialysis Transplantation 35, no. 12 (July 13, 2019): 2036–45. http://dx.doi.org/10.1093/ndt/gfz120.

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Abstract The cytoprotective transcriptor factor nuclear factor erythroid 2– related factor 2 (NRF2) is part of a complex regulatory network that responds to environmental cues. To better understand its role in a cluster of inflammatory and pro-oxidative burden of lifestyle diseases that accumulate with age, lessons can be learned from evolution, the animal kingdom and progeroid syndromes. When levels of oxygen increased in the atmosphere, mammals required ways to protect themselves from the metabolic toxicity that arose from the production of reactive oxygen species. The evolutionary origin of the NRF2–Kelch-like ECH-associated protein 1 (KEAP1) signalling pathway from primitive origins has been a prerequisite for a successful life on earth, with checkpoints in antioxidant gene expression, inflammation, detoxification and protein homoeostasis. Examples from the animal kingdom suggest that superior antioxidant defense mechanisms with enhanced NRF2 expression have been developed during evolution to protect animals during extreme environmental conditions, such as deep sea diving, hibernation and habitual hypoxia. The NRF2–KEAP1 signalling pathway is repressed in progeroid (accelerated ageing) syndromes and a cluster of burden of lifestyle disorders that accumulate with age. Compelling links exist between tissue hypoxia, senescence and a repressed NRF2 system. Effects of interventions that activate NRF2, including nutrients, and more potent (semi)synthetic NRF2 agonists on clinical outcomes are of major interest. Given the broad-ranging actions of NRF2, we need to better understand the mechanisms of activation, biological function and regulation of NRF2 and its inhibitor, KEAP1, in different clinical conditions to ensure that modulation of this thiol-based system will not result in major adverse effects. Lessons from evolution, the animal kingdom and conditions of accelerated ageing clarify a major role of a controlled NRF2–KEAP1 system in healthy ageing and well-being.

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Jolivet, Katell, Eric Grenier, Jean-Paul Bouchet, Magali Esquibet, Marie-Claire Kerlan, Bernard Caromel, Didier Mugniéry, and Véronique Lefebvre. "Identification of plant genes regulated in resistant potato Solanum sparsipilum during the early stages of infection by Globodera pallida." Genome 50, no. 4 (April 2007): 422–27. http://dx.doi.org/10.1139/g07-015.

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Using a complementary (c)DNA-amplified fragment length polymorphism (AFLP) approach, we investigated differential gene expression linked to resistance mechanisms during the incompatible potato – Globodera pallida interaction. Expression was compared between a resistant and a susceptible potato clone, inoculated or not inoculated with G. pallida. These clones were issued from a cross between the resistant Solanum sparsipilum spl329.18 accession and the susceptible dihaploid S. tuberosum Caspar H3, and carried, respectively, resistant and susceptible alleles at the resistance quantitative trait loci (QTLs). Analysis was done on root fragments picked up at 4 time points, during a period of 6 days after infection, from penetration of the nematode in the root to degradation of the feeding site in resistant plants. A total of 2560 transcript-derived fragments (TDFs) were analyzed, resulting in the detection of 46 TDFs that were up- or downregulated. The number of TDFs that were up- or downregulated increased with time after inoculation. The majority of TDFs were upregulated at only 1 or 2 time points in response to infection. After isolation and sequencing of the TDFs of interest, a subset of 36 sequences were identified, among which 22 matched plant sequences and 2 matched nematode sequences. Some of the TDFs that matched plant genes showed clear homologies to genes involved in cell-cycle regulation, transcription regulation, resistance downstream signalling pathways, and defense mechanisms. Other sequences with homologies to plant genes of unknown function or without any significant similarity to known proteins were also found. Although not exhaustive, these results represent the most extensive list of genes with altered RNA levels after the incompatible G. pallida–potato interaction that has been published to date. The function of these genes could provide insight into resistance or plant defense mechanisms during incompatible potato-cyst nematode interactions.

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Peng, Chieh Yu, Bang Jau You, Chia Lin Lee, Yang Chang Wu, Wen Hsin Lin, Te Ling Lu, Fei-Ching Chang, and Hong Zin Lee. "The Roles of 4β-Hydroxywithanolide E from Physalis peruviana on the Nrf2-Anti-Oxidant System and the Cell Cycle in Breast Cancer Cells." American Journal of Chinese Medicine 44, no. 03 (January 2016): 617–36. http://dx.doi.org/10.1142/s0192415x16500348.

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4[Formula: see text]-Hydroxywithanolide E is an active component of the extract of Physalis peruviana that has been reported to exhibit antitumor effects. Although the involvement of reactive oxygen species (ROS) production and the ataxia-telangiectasia mutated protein (ATM)-dependent DNA damage signaling pathway in 4[Formula: see text]-hydroxywithanolide E-induced apoptosis of breast cancer MCF-7 cells was demonstrated in our previous study, the relationship between ROS production and the cellular defense system response in 4[Formula: see text]-hydroxywithanolide E-induced cell death requires further verification. The present study suggests that ROS play an important role in 4[Formula: see text]-hydroxywithanolide E-induced MCF-7 cell death in which anti-oxidants, such as glutathione or N-acetylcysteine, can resist the 4[Formula: see text]-hydroxywithanolide E-induced accumulation of ROS and cell death. Furthermore, N-acetylcysteine or glutathione can reverse the 4[Formula: see text]-hydroxywithanolide E-induced changes in the cell cycle distribution and the expression of cell cycle regulators. We found that the 4[Formula: see text]-hydroxywithanolide E-induced ROS accumulation was correlated with the upregulation of Nrf2 and Nrf2-downstream genes, such as antioxidative defense enzymes. In general, the activity of Nrf2 is regulated by the Ras signalling pathway. However, we demonstrated that Nrf2 was activated during 4[Formula: see text]-hydroxywithanolide E-induced MCF-7 cell death in spite of the 4[Formula: see text]-hydroxywithanolide E-induced inhibition of the Ras/Raf/ERK pathway. The activity and protein expression of superoxide dismutase and catalase were involved in the 4[Formula: see text]-hydroxywithanolide E-induced ROS production in MCF-7 cells. Furthermore, 4[Formula: see text]-hydroxywithanolide E was demonstrated to significantly reduce the sizes of the tumor nodules in the human breast cancer MDA-MB231 xenograft tumor model.

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Ruxton, Graeme D., and Thomas N. Sherratt. "Aggregation, defence and warning signals: the evolutionary relationship." Proceedings of the Royal Society B: Biological Sciences 273, no. 1600 (May 23, 2006): 2417–24. http://dx.doi.org/10.1098/rspb.2006.3570.

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In a seminal contribution, Fisher argued how distastefulness could incrementally evolve in a prey species that was distributed in family groups. Many defended prey species occur in aggregations, but did aggregation facilitate the evolution of defence as Fisher proposed or did the possession of a defence allow individuals to enjoy the benefits of group living? Contemporary theory suggests that it can work both ways: pre-existing defences can make the evolution of gregariousness easier, but gregariousness can also aid the evolution of defence and warning signals. Unfortunately, the key phylogenetic analyses to elucidate the ordering of events have been hampered by the relative rarity of gregarious species, which in itself indicates that aggregation is not a pre-requisite for defence. Like the underlying theory, experimental studies have not given a definitive answer to the relative timing of the evolution of defence and aggregation, except to demonstrate that both orderings are possible. Conspicuous signals are unlikely to have evolved in the absence of a defence and aggregated undefended prey are likely to be vulnerable to predation in the absence of satiation effects. It therefore seems most likely that defence generally preceded the evolution of both aggregation and signalling, but alternative routes may well be possible.

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Lamichhane, A., V. Chaudhary, NK Sah, M. Singh, and R. Pandey. "Low Molecular Weight Antioxidants (LMWA) and their Orchestration." Nepal Journal of Medical Sciences 2, no. 2 (October 23, 2013): 171–80. http://dx.doi.org/10.3126/njms.v2i2.8971.

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Every day we hear more and more about free radicals and how they are linked with innumerable diseases and health conditions from ageing to muscular degeneration and even some forms of cancer. The problem is not in knowing that these microscopic enemies exist. We know that they do! The problem is how to fight them so that they are rendered harmless. Under normal metabolic conditions each cell of human body is exposed to about 1010 molecules of superoxide anions (primary free radical) each day. For a person weighing 150 pounds, this amounts to about 4 pounds of superoxide per year, a substantial amount! Once formed, superoxide can react through catalytic pathways in the cell to form many other reactive oxygen/nitrogen species (ROS/RNS). The antioxidant defense system in the human body is extensive and consists of multiple layers, which protect against different types of ROS/RNS. Many of the biological effects of antioxidants appear to be related to their ability not only to scavenge the deleterious free radicals but also to modulate cell signalling pathways. Nepal Journal of Medical Sciences | Volume 02 | Number 02 | July-December 2013 | Page 171-180 DOI: http://dx.doi.org/10.3126/njms.v2i2.8971

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Taiwe, Germain Sotoing, Arielle Larissa Ndieudieu Kouamou, Bernard Dabole, Armelle Rosalie Mbang Ambassa, Hart Mann Alain Youbi Mambou, Raymond Bess Bila, Thierry Bang Tchoya, Joseph Renaud Menanga, Paul Desire Djomeni Dzeufiet, and Elisabeth Ngo Bum. "Protective Effects of Anthocleista djalonensis Extracts against Pentylenetetrazole-Induced Epileptic Seizures and Neuronal Cell Loss: Role of Antioxidant Defense System." Evidence-Based Complementary and Alternative Medicine 2021 (August 30, 2021): 1–18. http://dx.doi.org/10.1155/2021/5523705.

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Oxidative stress and neurodegeneration are involved in the initiation of epileptogenesis and progression of epileptic seizures. This study was aimed at investigating the anticonvulsant, antioxidant, and neuroprotective properties of active fractions isolated from Anthocleista djalonensis root barks in pentylenetetrazole mouse models of epileptic seizures. Bioactive-guided fractionation of Anthocleista djalonensis (AFAD) extracts using acute pentylenetetrazole (90 mg/kg) induced generalised tonic-clonic seizures, which afforded a potent anticonvulsant fraction (FPool 5). Further fractionation of AFAD was performed by high-performance liquid chromatography, which yielded fifteen subfractions, which were chemically characterised. In addition, AFAD was tested against convulsions or spontaneous kindled seizures induced, respectively, by acute (50 mg/kg) or subchronic (30 mg/kg) injection of pentylenetetrazole. Finally, oxidative stress markers, brain GABA content, and neuronal cell loss were evaluated in AFAD-treated pentylenetetrazole-kindled mice. Administration of AFAD significantly protected mice against acute pentylenetetrazole (90 mg/kg)-induced convulsions. In acute pentylenetetrazole (50 mg/kg)-induced hippocampal and cortical paroxysmal discharges, AFAD significantly decreased the number of crisis, the cumulative duration of crisis, and the mean duration of crisis. Additionally, AFAD significantly decreased the number of myoclonic jerks and improved the seizure score in subchronic pentylenetetrazole-induced kindled seizures. The pentylenetetrazole-induced alteration of oxidant-antioxidant balance, GABA concentration, and neuronal cells in the brain were attenuated by AFAD treatment. This study showed that AFAD protected mice against pentylenetetrazole-induced epileptic seizures possibly through the enhancement of antioxidant defence and GABAergic signalling. These events might be correlated with the amelioration of neuronal cell loss; hence, AFAD could be a potential candidate for the treatment of epilepsy.

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Rayet, Béatrice, José-Antonio Lopez-Guerrero, Jean Rommelaere, and Christiane Dinsart. "Induction of Programmed Cell Death by Parvovirus H-1 in U937 Cells: Connection with the Tumor Necrosis Factor Alpha Signalling Pathway." Journal of Virology 72, no. 11 (November 1, 1998): 8893–903. http://dx.doi.org/10.1128/jvi.72.11.8893-8903.1998.

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ABSTRACT The human promonocytic cell line U937 undergoes apoptosis upon treatment with tumor necrosis factor alpha (TNF-α). This cell line has previously been shown to be very sensitive to the lytic effect of the autonomous parvovirus H-1. Parvovirus infection leads to the activation of the CPP32 ICE-like cysteine protease which cleaves the enzyme poly(ADP-ribose)polymerase and induces morphologic changes that are characteristic of apoptosis in a way that is similar to TNF-α treatment. This effect is also observed when the U937 cells are infected with a recombinant H-1 virus which expresses the nonstructural (NS) proteins but in which the capsid genes are replaced by a reporter gene, indicating that the induction of apoptosis can be assigned to the cytotoxic nonstructural proteins in this cell system. The c-Myc protein, which is overexpressed in U937 cells, is rapidly downregulated during infection, in keeping with a possible role of this product in mediating the apoptotic cell death induced by H-1 virus infection. Interestingly, four clones (designated RU) derived from the U937 cell line and selected for their resistance to H-1 virus (J. A. Lopez-Guerrero et al., Blood 89:1642–1653, 1997) failed to decrease c-Myc expression upon treatment with differentiation agents and also resisted the induction of cell death after TNF-α treatment. Our data suggest that the RU clones have developed defense strategies against apoptosis, either by their failure to downregulate c-Myc and/or by activating antiapoptotic factors.

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Nunez, Steven C., Thomas A. Jenssen, and Kasey Ersland. "Female Activity Profile of a Polygynous Lizard (Anolis Carolinensis): Evidence of Intersexual Asymmetry." Behaviour 134, no. 3-4 (1997): 205–23. http://dx.doi.org/10.1163/156853997x00458.

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Abstract1. The activity profile of free-ranging individuals should reflect how females and males are optimizing their respective reproductive efforts. By using the polygynous, sexually dimorphic lizard, Anolis carolinensis, we expected to find an example of pronounced intersexual asymmetry in daily activity patterns. 2. In contrast to males who should focus on blocking consexual access to resident females, we expected females to strategically facilitate egg production by minimizing conspicuous and unnecessary behavior, while feeding frequently from a defended food resource optimal to their needs. 3. During a 56 day period, we made a 90 h record of focal animal observations on 22 unmanipulated, reproductive females; then we compared this activity profile to a known profile for males. We found the following. 4. Females were 1.6 times more stationary (82% of day), moved 1/7th the distance (< 40 m/day), displayed at 1/8th the overall rate (< 14 displays/h), and used < 1/35th the number of displays in non-directed advertisement (1.6 displays/h) as males. 5. Females spent 1/30th the time (0.3% of day) in overt defense of territories 1/9th the volume (8 m3) as males. 6. However, both females and males had equivalent feeding rates (1.2 times/h), suggesting that the energetic needs of female egg production and male territorial maintenance are comparable. 7. The small, lightly defended territories and low feeding rates of females (along with their reptilian metabolism and insectivorous diet) indicate that females have a wide latitude in which to meet their energetic costs. 8. As expected, the proportion of intersexual contacts was similar between female and male profiles. Courtship and copulations occupied 3.2% and 3.9% of the females' day, respectively, with copula averaging 26 min in duration. 9. In a female activity profile which de-emphasized conspicuousness, we found little evidence for a pheromone-based alternative to visual signalling. 10. Predation, as an immediate threat to lizard activities, was not seen during three months of observations. We noted only four instances of avoidance behavior.

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Zhang, Yuanyuan, Harro J. Bouwmeester, and Iris F. Kappers. "Combined transcriptome and metabolome analysis identifies defence responses in spider mite-infested pepper (Capsicum annuum)." Journal of Experimental Botany 71, no. 1 (September 26, 2019): 330–43. http://dx.doi.org/10.1093/jxb/erz422.

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Abstract Plants regulate responses towards herbivory through fine-tuning of defence-related hormone production, expression of defence genes, and production of secondary metabolites. Jasmonic acid (JA) plays a key role in plant–herbivorous arthropod interactions. To understand how pepper (Capsicum annuum) responds to herbivory, leaf transcriptomes and metabolomes of two genotypes different in their susceptibility to spider mites were studied. Mites induced both JA and salicylic acid (SA) signalling. However, mite infestation and exogenous JA resulted in distinct transcriptome profiles. Compared with JA, mites induced fewer differentially expressed genes involved in metabolic processes (except for genes involved in the phenylpropanoid pathway) and lipid metabolic processes. Furthermore, pathogen-related defence responses including WRKY transcription factors were more strongly induced upon mite infestation, probably as a result of induced SA signalling. Untargeted analysis of secondary metabolites confirmed that JA treatment induced larger changes in metabolism than spider mite infestation, resulting in higher terpenoid and flavonoid production. The more resistant genotype exhibited a larger increase in endogenous JA and volatile and non-volatile secondary metabolites upon infestation, which could explain its stronger defence. Reasoning that in JA–SA antagonizing crosstalk, SA defences are prioritized over JA defences, we hypothesize that lack of SA-mediated repression of JA-induced defences could result in gain of resistance towards spider mites in pepper.

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Zhou, Ying, Lanting Zeng, Xingliang Hou, Yinyin Liao, and Ziyin Yang. "Low temperature synergistically promotes wounding-induced indole accumulation by INDUCER OF CBF EXPRESSION-mediated alterations of jasmonic acid signaling in Camellia sinensis." Journal of Experimental Botany 71, no. 6 (January 4, 2020): 2172–85. http://dx.doi.org/10.1093/jxb/erz570.

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Abstract Plants have to cope with various environmental stress factors which significantly impact plant physiology and secondary metabolism. Individual stresses, such as low temperature, are known to activate plant volatile compounds as a defense. However, less is known about the effect of multiple stresses on plant volatile formation. Here, the effect of dual stresses (wounding and low temperature) on volatile compounds in tea (Camellia sinensis) plants and the underlying signalling mechanisms were investigated. Indole, an insect resistance volatile, was maintained at a higher content and for a longer time under dual stresses compared with wounding alone. CsMYC2a, a jasmonate (JA)-responsive transcription factor, was the major regulator of CsTSB2, a gene encoding a tryptophan synthase β-subunit essential for indole synthesis. During the recovery phase after tea wounding, low temperature helped to maintain a higher JA level. Further study showed that CsICE2 interacted directly with CsJAZ2 to relieve inhibition of CsMYC2a, thereby promoting JA biosynthesis and downstream expression of the responsive gene CsTSB2 ultimately enhancing indole biosynthesis. These findings shed light on the role of low temperature in promoting plant damage responses and advance knowledge of the molecular mechanisms by which multiple stresses coordinately regulate plant responses to the biotic and abiotic environment.

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Zuo, Xu, Yinuo Gu, Chao Wang, Jinrong Zhang, Jing Zhang, Guoqiang Wang, and Fang Wang. "A Systematic Review of the Anti-Inflammatory and Immunomodulatory Properties of 16 Essential Oils of Herbs." Evidence-Based Complementary and Alternative Medicine 2020 (December 7, 2020): 1–14. http://dx.doi.org/10.1155/2020/8878927.

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Background. Inflammation is a host defense mechanism in the body after it is infected and damaged. If inflammation is not treated in time, then it may cause a variety of diseases, such as cancer and autoimmune diseases. Herbal essential oils are natural extracts that can suppress inflammation effectively and are expected to be used in therapeutic drugs for anti-inflammatory diseases in the future. Aim of the review. We review the anti-inflammatory and immunomodulatory effects of essential oils derived from 16 herbs. Materials and methods. We searched the literature of the fields of anti-inflammatory and immunomodulatory herbal essential oil activity published in English within the past five years via databases (PubMed, EMBASE, Scopus, and The Web of Science). Results. A total of 1932 papers were found by searching, and 132 papers were screened after removing duplicates and reading article titles. Fifteen articles met the requirements to be included in this review. Among those selected, 11 articles reported in vivo research results, and 10 articles showed research results. Conclusion. Essential oils extracted from herbs can reduce inflammation by regulating the release of inflammatory cytokines involved in multiple signalling pathways. Herbal essential oils are expected to be developed as anti-inflammatory drugs.

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Broom, M., M. P. Speed, and G. D. Ruxton. "Evolutionarily stable defence and signalling of that defence." Journal of Theoretical Biology 242, no. 1 (September 2006): 32–43. http://dx.doi.org/10.1016/j.jtbi.2006.01.032.

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Miranda-Díaz, Alejandra Guillermina, José Manuel Hermosillo-Sandoval, Martha Arisbeth Villanueva-Pérez, Luis Miguel Román-Pintos, Trinidad García-Iglesias, Adolfo Daniel Rodríguez-Carrizalez, and Ernesto Germán Cardona-Muñoz. "Toll-Like Receptor-1 and Receptor-2 and Beta-Defensin in Postcholecystectomy Bile Duct Injury." Gastroenterology Research and Practice 2015 (2015): 1–6. http://dx.doi.org/10.1155/2015/216129.

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Postcholecystectomy bile duct injuries (BDI) produce hepatic cholestasis and cause infection of the biliary tract. The biliary cells participate in secreting cytokines and in expression of immune response receptors. Toll-like receptors (TLRs) conduct signalling and activate the innate and adaptive inflammatory response. The objective was to determine the serum levels of TLR-2 and the expression of TLR-1 and TLR-2 andβ-defensin in liver biopsies of postcholecystectomy BDI patients. A transverse, analytical study with 2 groups was done. One group included healthy volunteers (control group) and other included 25 postcholecystectomy BDI patients with complete biliary obstruction. Using the Enzyme-linked Immunosorbent Assay (ELISA) technique, serum levels of TLR-2 were determined, and with immunofluorescence the morphologic analysis of TLR-1 and TLR-2 andβ-defensin in liver biopsies of postcholecystectomy BDI patients was performed. The average TLR-2 serum level in the control group was 0.0 pg/mL and in the BDI group,0.023±0.0045 pg/mL(P<0.0001, bilateral Mann WhitneyU). Immunofluorescence was used to determine the expression in liver biopsies, blood vessels, bile ducts, and hepatic parenchyma where 12 hepatic biopsies were positive for TLR-1 with average of3213057.74±1071019.25 μm2; and 7 biopsies were positive forβ-defensin with an average of730364.33±210838.02 μm2; and 6 biopsies positive for TLR-2, obtaining an average of3354364.24±838591.06 μm2. In conclusion, TLR-1 and TLR-2 andβ-defensin play an important role in the innate antimicrobial defense of the hepatobiliary system.

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Ratcliffe, Laurene, and Daniel Mennill. "Do Male Black-capped Chickadees Eavesdrop on Song Contests? A Multi-speaker Playback Experiment." Behaviour 141, no. 1 (2004): 125–39. http://dx.doi.org/10.1163/156853904772746637.

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AbstractWithin a network of communicating individuals, animals may gather information about the relative quality of conspecifics by eavesdropping on their signalling interactions. For territorial male songbirds, eavesdropping may be a low-cost, low-risk method for assessing the relative quality of the males around them. We used a three-speaker playback design to evaluate whether male black-capped chickadees (Poecile atricapillus) respond differently to two simulated countersinging intruders who differ only in relative features of their singing performance. We arranged three loudspeakers in an equilateral triangle at the center of playback subjects' territories. After luring males to the first loudspeaker by broadcasting non-song vocalizations, we played songs from the remaining loudspeakers to simulate a countersinging interaction between two male intruders. During the interactions, one simulated intruder consistently overlapped the songs of the other, a behaviour thought to be a signal of directed aggression in songbirds. Territorial male chickadees discriminated between the simulated intruders by preferentially approaching the loudspeaker broadcasting the overlapping signal, suggesting that males eavesdrop on other males' countersinging interactions. Male responses to playback support the idea that overlapping is a more threatening signal than being overlapped. Responses varied with the dominance status of the subject. High-ranking males approached the overlapping loudspeaker in 15 of 16 cases whereas low-ranking males approached the overlapping speaker in only 5 of 10 cases, suggesting that males of different quality may use different tactics for territorial defense.

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Journal articles on the topic 'Defense signalling'

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